This is a working overview of Cardarine, written for readers who want more than a one-paragraph summary but less than a textbook.
This page was last updated on 2026-06-18 and is reviewed periodically as new material appears.
Preclinical research reported that GW501516 increased running endurance in mice and improved lipid profiles in some animal species. Early human trials explored effects on high-density lipoprotein cholesterol, triglycerides, and glucose handling, but the program was discontinued. Published human data are sparse and do not establish efficacy for any condition. Studies also examined PPAR delta in cancer biology, with conflicting findings across models. The relationship between receptor activation, tissue context, and disease risk remains an active area of investigation.
Anti-doping laboratories identify GW501516 and its metabolites using liquid chromatography-tandem mass spectrometry. Urine is the usual matrix, and detection can occur after the parent compound has cleared from blood. The exact detection window depends on dose, formulation, individual metabolism, and assay sensitivity. Because the compound is prohibited at all times, athletes are subject to testing in and out of competition. Analytical methods continue to improve as new metabolites and designer analogs are characterized.
GW501516 acts as an agonist at the peroxisome proliferator-activated receptor delta, a nuclear receptor that regulates gene expression. Activation shifts transcription toward genes involved in fatty acid uptake, oxidation, and energy expenditure. The compound does not bind the androgen receptor and therefore differs from anabolic steroids and SARMs. In rodent models, this metabolic shift has been linked to increased running endurance and reduced fat accumulation. The exact downstream pathways in humans remain incompletely characterized.
Early clinical research explored GW501516 for lipid disorders, obesity, and diabetes. Some short-term human studies reported changes in HDL cholesterol, LDL cholesterol, and triglycerides. The development program was discontinued after rodent studies showed dose-dependent tumor formation in multiple tissues, including liver, bladder, stomach, and skin. These findings raised concerns about long-term cancer risk in humans. Because human exposure data are limited, the clinical significance of the rodent tumors remains uncertain.
| Property | Value | Notes |
|---|---|---|
| Molecular target | PPAR delta (NR1C2) | Ligand-activated nuclear receptor. |
| Primary tissues studied | Skeletal muscle, liver, adipose | Effects on fatty acid oxidation and energy use. |
| Typical detection matrix | Urine | Used in anti-doping analysis. |
| Common analytical method | LC-MS/MS | Detects parent compound and metabolites. |
| Sport regulatory class | Prohibited at all times | Listed as a metabolic modulator by WADA. |
Cardarine is a common name for GW501516, also GW-1516, a synthetic compound developed as a peroxisome proliferator-activated receptor delta (PPARδ) agonist. It belongs to a class of agents that modulate gene transcription related to lipid and energy metabolism. The compound was studied in preclinical and early clinical research for metabolic and cardiovascular conditions, but it did not progress to approved therapeutic use. Its name appears in fitness and sports contexts despite not being approved as a drug.
PPARδ is a nuclear receptor that influences transcription of genes involved in fatty acid oxidation, lipid transport, and energy homeostasis. GW501516 binds and activates this receptor with high selectivity relative to PPARα and PPARγ in laboratory assays. Activation alters expression of target genes in skeletal muscle, liver, and adipose tissue in animal models. The exact clinical consequences of these changes in humans remain incompletely characterized, and observed effects in animals do not establish therapeutic benefit or safety.
Published studies have examined GW501516 in animal models of obesity, insulin resistance, and exercise endurance. Early human trials reportedly ended, and development was discontinued after preclinical findings raised concerns about cancer in some rodent studies. Regulatory agencies have not approved cardarine for any medical use. Its availability through non-pharmaceutical channels raises questions about identity, purity, and legal status that are separate from its laboratory pharmacology. Those questions are often addressed through analytical testing rather than assumptions about product labels.
Cardarine is not approved for human therapeutic use in any major jurisdiction. It appears on the World Anti-Doping Agency Prohibited List as a PPARδ agonist within the hormone and metabolic modulators category. Sports organizations test for it because it has been detected in athlete samples and seized products. Regulatory actions against marketed research chemical versions have occurred in several countries, though enforcement varies. Availability through unregulated channels complicates oversight.
Analytical laboratories typically identify cardarine and its metabolites using liquid chromatography-tandem mass spectrometry. Urine is a common matrix in anti-doping testing, while blood and tissue may be used in research settings. Detection windows depend on the assay, the sample matrix, and the compound's metabolism. Because cardarine is extensively metabolized, laboratories often target specific metabolites to improve sensitivity and confirmation. Reference standards are required for reliable quantification. Method validation includes checks for selectivity, linearity, and carryover.
GW501516 binds and activates PPARδ, a nuclear receptor that influences transcription of genes involved in fatty acid oxidation and energy use. Activation shifts some metabolic pathways in preclinical models, which is why the compound has been studied for lipid disorders and exercise-related endpoints. The exact downstream effects in humans are incompletely mapped. PPARδ is expressed in many tissues, including skeletal muscle, liver, and adipose tissue, so broad activation may have varied consequences. Researchers continue to examine how selective or partial activation might alter the balance between benefits and risks.
Published human data are sparse and mostly come from early-phase trials. Those studies examined short-term changes in lipids, glucose, and exercise capacity, but they were not large enough to establish efficacy or long-term safety. Some animal experiments reported increased running endurance, yet such findings do not prove a performance benefit in people. Anti-doping laboratories detect GW501516 and its metabolites in urine or blood using liquid chromatography-tandem mass spectrometry. Detection windows depend on dose, sample type, and individual metabolism. The method is sensitive enough to identify trace residues in tested samples.
== Causes == Most presentations of CTS have no known disease cause (idiopathic). The association of other factors with CTS is a source of notable debate. It is important to distinguish factors that provoke symptoms and factors that are associated with seeking care from factors that make the neuropathy worse. Genetic factors are believed to be the most important determinants of who develops carpal tunnel syndrome. In other words, one's wrist structure seems programmed at birth to develop CTS later in life. A genome-wide association study (GWAS) of carpal tunnel syndrome identified 50 genomic loci significantly associated with the disease, including several loci previously known to be associated with human height. Some other factors that contribute to carpal tunnel syndrome are conditions such as diabetes, alcoholism, vitamin deficiency or toxicity as well as exposure to toxins. Conditions such as these don't necessarily increase the interstitial pressure of the carpal tunnel. One case-control study noted that individuals classified as obese (BMI >29) are 2.5 times more likely than slender individuals (BMI <20) to be diagnosed with CTS. It is not clear whether this association is due to an alteration of pathophysiology, a variation in symptoms, or a variation in care-seeking.
DMF penetrates most plastics and makes them swell. Because of this property DMF is suitable for solid phase peptide synthesis and as a component of paint strippers. DMF is used as a solvent to recover olefins such as 1,3-butadiene via extractive distillation. It is used in the manufacturing of solvent dyes as an important raw material. It is consumed during reaction. Pure acetylene gas cannot be compressed and stored without the danger of explosion. Industrial acetylene is safely compressed in the presence of dimethylformamide, which forms a safe, concentrated solution. The casing is also filled with agamassan, which renders it safe to transport and use. As a cheap and common reagent, DMF has many uses in a research laboratory.
== External links == Calvete JJ (1995). "On the structure and function of platelet integrin alpha IIb beta 3, the fibrinogen receptor". Proc. Soc. Exp. Biol. Med. 208 (4): 346–60. doi:10.3181/00379727-208-43863a. PMID 7535429. Garner Stephen F., Campbell Kate, Metcalfe Paul, Keidan Jane, Huiskes Elly, Dong Jing-Fei, Lopez Jose A., Ouwehand Willem H. (2002). "Glycoprotein V: the predominant target antigen in gold-induced autoimmune thrombocytopenia" (PDF). Blood. 100 (1): 344–346. doi:10.1182/blood.V100.1.344. PMID 12070047.{{cite journal}}: CS1 maint: multiple names: authors list (link) Dumin J A, Dickeson S K, Stricker T P, Bhattacharyya-Pakrasi M, Roby J D, Santoro S A, Parks W C (2001). "Pro-collagenase-1 (matrix metalloproteinase-1) binds the alpha(2)beta(1) integrin upon release from keratinocytes migrating on type I collagen". J. Biol. Chem. 276 (31): 29368–74. doi:10.1074/jbc.M104179200. PMID 11359786.{{cite journal}}: CS1 maint: multiple names: authors list (link) http://www.reference.md/files/D019/mD019038.html Online Medical Dictionary, Platelet membrane glycoproteins Platelet+membrane+glycoproteins at the U.S. National Library of Medicine Medical Subject Headings (MeSH) http://www.ojrd.com/content/1/1/46/figure/F1?highres=y http://circ.ahajournals.org/content/99/1/e1/F4.large.jpg
Sources: en.wikipedia.org
== Function == Collagen VI plays many different roles in the cell depending on which tissue in which it is expressed. ColVI maintains a mechanical function in the cell, which is typical of most types of Collagen, by providing stability and structural support in the ECM. ColVI allows muscle cells to connect with the ECM by interacting with perlecan in the basal lamina. ColVI also functions as a cytoprotective agent:
== Treatment == Early and effective treatment of acne scarring can prevent severe acne and the scarring that often follows. In 2004, no prescription drugs for the treatment or prevention of scars were available.
Alport syndrome - hereditary kidney disease is distinguished by structural abnormalities and malfunction in the glomerular basement membrane, as well as basement membranes in other organs such as the eye and ear. Congenital contractural arachnodactyly - autosomal dominant disorder defined by arachnodactyly, multiple flexion contractures, abnormal pinnae, severe kyphoscoliosis, and muscular hypoplasia. Epidermolysis bullosa - hereditary, diverse grouping of rare genetic dermatoses that are marked by blisters and mucocutaneous fragility. Loeys–Dietz syndrome - autosomal dominant condition linked to a wide range of systemic manifestations, such as skeletal, cutaneous, vascular, and craniofacial abnormalities. Hypermobility spectrum disorder - a variety of connective tissue diseases that are marked by ongoing pain and joint hypermobility. Arterial tortuosity syndrome - a rare connective tissue disorder distinguished by abnormal twisting of the large arteries. Other features include marfanoid habitus, keratoconus, hypotonia, and bowel dilatations and perforations.
Sources: en.wikipedia.org
It binds to and activates PPAR delta, a nuclear receptor that controls expression of genes related to fatty acid oxidation. This mechanism can alter energy metabolism in animal models. It is not a direct stimulant or fat-burning enzyme.
Early-stage trials examined lipid and glucose markers, but the development program was discontinued. Published human results are limited and do not support approved use for any indication. Claims of performance or health benefits remain unproven.
Yes. Laboratories use LC-MS/MS to detect GW501516 and its metabolites in urine. Detection depends on timing and sensitivity, but the substance is banned at all times.
It targets PPARδ, a nuclear receptor involved in lipid and energy metabolism. It does not act primarily on androgen receptors. This distinction separates it from SARMs.